Interferon alfacon 1 inhibits SARS-CoV infection in human bronchial epithelial Calu-3 cells.
Identifieur interne : 001B72 ( PubMed/Curation ); précédent : 001B71; suivant : 001B73Interferon alfacon 1 inhibits SARS-CoV infection in human bronchial epithelial Calu-3 cells.
Auteurs : Yohichi Kumaki [États-Unis] ; Craig W. Day ; Miles K. Wandersee ; Bradley P. Schow ; Justin S. Madsen ; Dixon Grant ; Jason P. Roth ; Donald F. Smee ; Lawrence M. Blatt ; Dale L. BarnardSource :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2008.
Descripteurs français
- KwdFr :
- Animaux, Antiviraux (pharmacologie), Antiviraux (usage thérapeutique), Bronches (virologie), Humains, Interféron alpha, Interféron de type I (pharmacologie), Interféron de type I (usage thérapeutique), Lignée cellulaire, Lignée cellulaire tumorale, Muqueuse respiratoire (virologie), Protéines recombinantes, Réplication virale (), Syndrome respiratoire aigu sévère (traitement médicamenteux), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (), Virus du SRAS (physiologie).
- MESH :
- pharmacologie : Antiviraux, Interféron de type I.
- physiologie : Virus du SRAS.
- traitement médicamenteux : Syndrome respiratoire aigu sévère.
- usage thérapeutique : Antiviraux, Interféron de type I.
- virologie : Bronches, Muqueuse respiratoire, Syndrome respiratoire aigu sévère.
- Animaux, Humains, Interféron alpha, Lignée cellulaire, Lignée cellulaire tumorale, Protéines recombinantes, Réplication virale, Virus du SRAS.
English descriptors
- KwdEn :
- Animals, Antiviral Agents (pharmacology), Antiviral Agents (therapeutic use), Bronchi (virology), Cell Line, Cell Line, Tumor, Humans, Interferon Type I (pharmacology), Interferon Type I (therapeutic use), Interferon-alpha, Recombinant Proteins, Respiratory Mucosa (virology), SARS Virus (drug effects), SARS Virus (physiology), Severe Acute Respiratory Syndrome (drug therapy), Severe Acute Respiratory Syndrome (virology), Virus Replication (drug effects).
- MESH :
- chemical , pharmacology : Antiviral Agents, Interferon Type I.
- chemical , therapeutic use : Antiviral Agents, Interferon Type I.
- drug effects : SARS Virus, Virus Replication.
- drug therapy : Severe Acute Respiratory Syndrome.
- physiology : SARS Virus.
- virology : Bronchi, Respiratory Mucosa, Severe Acute Respiratory Syndrome.
- Animals, Cell Line, Cell Line, Tumor, Humans, Interferon-alpha, Recombinant Proteins.
Abstract
The primary targets for SARS-CoV infection are the epithelial cells in the respiratory and intestinal tract. The angiotensin-converting enzyme 2 (ACE-2) has been identified as a functional receptor for SARS-CoV. ACE-2 has been shown to be expressed at the apical domain of polarized Calu-3 cells. In this report, interferon alfacon 1 was examined for inhibitory activities against SARS-CoV on human lung carcinoma epithelial Calu-3 cell line and the other three African green monkey kidney epithelial cell lines. Interferon alfacon 1 demonstrated significant antiviral activity in neutral red uptake assay and virus yield reduction assay. The data might provide an important insight into the mechanism of pathogenesis of SARS-CoV allowing further development of antiviral therapies for treating SARS infections.
DOI: 10.1016/j.bbrc.2008.04.006
PubMed: 18406349
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pubmed:18406349Le document en format XML
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<front><div type="abstract" xml:lang="en">The primary targets for SARS-CoV infection are the epithelial cells in the respiratory and intestinal tract. The angiotensin-converting enzyme 2 (ACE-2) has been identified as a functional receptor for SARS-CoV. ACE-2 has been shown to be expressed at the apical domain of polarized Calu-3 cells. In this report, interferon alfacon 1 was examined for inhibitory activities against SARS-CoV on human lung carcinoma epithelial Calu-3 cell line and the other three African green monkey kidney epithelial cell lines. Interferon alfacon 1 demonstrated significant antiviral activity in neutral red uptake assay and virus yield reduction assay. The data might provide an important insight into the mechanism of pathogenesis of SARS-CoV allowing further development of antiviral therapies for treating SARS infections.</div>
</front>
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